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Equine Medicine > Muscle Diseases, Pt. 2 > Flashcards

Muscle Diseases, Pt. 2 Flashcards

1
Q

Etiologies of myopathy and rhabdomyolysis:

A
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2
Q

What is the difference between rhabdomyolysis and myopathy?

A

RHABDO = disruption of skeletal muscle integrity with myalgia, weakness, myoglobinuria, and significant increase in muscle enzymes - acute kidney disease is common

MYOPATHY = general term to describe muscle disease with more subtle clinical signs and NO increase in muscle enzymes

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3
Q

What is the most common cause of Clostridial myositis? How do horses become infected?

A

C. perfringens > C. septicum, chauvoei, and sporogenes

invasion of the G+, anaerobic bacteria into the deep muscle by IM injection or penetrating wounds allows for rapid division and toxin production due to the low amount of oxygen

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4
Q

Which IM drug has Clostridial myositis been associated with?

A

Banamine (flunixin meglumine)

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5
Q

What 4 local signs are associated with Clostridial myositis?

A
  1. swollen, hot, discolored area becomes cool, insensitive, and sloughs
  2. crepitus - “crunchy”
  3. malodorous serosanguinous fluid
  4. “cooked” muscle appearance
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6
Q

What general signs are associated with Clostridial myositis?

A
  • depression
  • fever
  • toxemia (injected MM, increased CRT)
  • tremors, ataxia
  • dyspnea
  • recumbency, coma, death
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7
Q

What 4 things are diagnostic of Clostridial myositis on CBC and biochemistry?

A
  1. hemoconcentration
  2. stress leukogram
  3. toxemia
  4. increased CK and AST
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8
Q

What is seen on ultrasound and aspirates in cases of Clostridial myositis?

A

fluid and hyperechoic gas accumulation

rod-shaped bacteria on anaerobic culture

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9
Q

What kinds of antimicrobials are used in cases of Clostridial myositis? What route(s) of administration would be preferred?

A

ones that work on G+ anaerobes - Penicillin!

  • IV*
  • IM is acceptable, but there is already extensive muscle damage
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10
Q

What are the 2 antimicrobials recommended for treating Clostridial myositis? What surgical treatment is done?

A
  1. potassium Penicillin (q 2-4 hr)
  2. Metronidazole

debridement and fenestration - gets rid of devitalized tissue, introduces oxygen, and allows for drainage

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11
Q

What supportive treatment is recommended for Clostridial myositis? What is prognosis like?

A
  • fluids
  • NSAIDs
  • steroids

guarded to poor

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12
Q

What is the etiology of myosin-heavy chain myopathy (MyHM)? In what horses is this most common?

A

autosomal codominant mutation in MyHM1 gene in type 2 X fibers, causing the immune system to attack the altered myosin chains

<8 or >17 y/o reigning and cutting QH

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13
Q

What are the most common triggers of myosin-heavy chain myopathy (MyHM)? 2 clinical presentations?

A

respiratory infection and vaccinations

  1. immune-mediated myositis
  2. non-exertional rhabdomyolsis
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14
Q

What is the most common cause of rapid atrophy of the topline in AQH and APH?

A

myosin-heavy chain myopathy (MyHM)

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15
Q

What 2 clinical signs are associated with immune-mediated myositis from myosin-heavy chain myopathy (MyHM)?

A
  1. rapid muscle atrophy of epaxial and gluteal muscles (topline)
  2. stiffness, weakness, malaise
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16
Q

What 3 clinical signs are associated with rhabdomyolysis from myosin-heavy chain myopathy (MyHM)?

A
  1. pain, reluctance to move
  2. myoglobinuria
  3. increased muscle enzymes

(more severe form!)

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17
Q

What are the 3 ways to diagnose myosin-heavy chain myopathy (MyHM)?

A
  1. CK and AST 10,000 IU (higher if rhabdomyolysis)
  2. genetic testing
  3. muscle biopsy (not commonly done)
18
Q

What are the top differentials associated with myosin-heavy chain myopathy (MyHM)?

A
  • EMND, neurogenic muscle atrophy
  • causes of cachexia
  • PPID
  • PSSM1
19
Q

What elevation in CK may we expect with rhabdomyolysis?

A

> 10,000 IU (can get up to 100,000)

  • very significant and severe
20
Q

What medical treatment is recommended for myosin-heavy chain myopathy (MyHM)?

A
  • Dexamethasone for 3 days, followed by tapered Prednisolone for 7-10 days
  • treat rhabdomyolysis with IV fluids and NSAIDs

monitor CBC!

21
Q

What are 3 additional treatments recommended for myosin-heavy chain myopathy (MyHM)?

A
  1. balanced nutrition concentrating on high-quality proteins
  2. extend time between vaccines
  3. avoid Strangles vaccine —> purpura hemorrhagica!
22
Q

What is the prognosis of myosin-heavy chain myopathy (MyHM) like?

A

HETEROZYGOUS - muscle mass returns in 2-3 months with treatment

HOMOZYGOUS - atrophy more severe and recurrence possible

23
Q

What are the most common causes of white muscle disease in mares and foals?

A

MARES - deficient vitamin E and selenium

FOALS - natural in young and fast-growing animals, not enough vitamin E or selenium from mare

24
Q

In what 3 environments is deficient selenium most common?

A
  1. rapidly growing fertilized plants
  2. poorly aerated acidic soil
  3. volcanic rock
25
Q

What are 2 dietary causes of deficient vitamin E?

A
  1. no grass or poor-quality hay
  2. heated pelleted feed
26
Q

What are signs of subacute nutritional myodegeneration?

A
  • weakness
  • dysphagia, aspiration pnuemonia
  • stiffness, trembling, firm muscles
  • difficulty rising
27
Q

What are signs of acute nutritional myodegeneration?

A
  • rapidly progressive weakness, recumbency, or death
  • large muscle groups affected
  • tachycardia, arrhythmia, murmurs
  • respiratory distress, pulmonary edema, aspiration pneumonia
28
Q

How does the type of muscle cause differences in signs of nutritional myodegeneration?

A

SKELETAL = slower onset of weakness, stiffness, trembling, recumbency, and dysphagia

CARDIAC = acute myocardial decompensation

29
Q

What 7 muscles are most commonly affected by skeletal muscle nutritional myodegeneration?

A
  1. gastrocnemius
  2. semimembranosus
  3. biceps
  4. lumbar, gluteal, and neck regions
  5. diaphragm
  6. intercostal
  7. tongue
30
Q

What are 5 signs on clinical pathology in nutritional myodegeneration?

A
  1. increased muscle enzymes
  2. low whole blood Se or vitamin E
  3. increased potassium, phosphorus, and sodium
  4. decreased chloride and calcium
  5. dehydration
31
Q

What enzyme can be found in RBCs in cases of nutritional myodegeneration?

A

glutathione peroxidase (GSH-Px)

32
Q

What pathology is seen in tissues in cases of nutritional myodegeneration?

A
  • bilaterally symmetric myodegeneration
  • myonecrosis
33
Q

What 3 treatments are recommended for nutritional myodegeneration?

A
  1. supportive care - stall rest
  2. treat deficiency - Se IM, oral vit E in water
  3. control complications
34
Q

How can nutritional myodegeneration be prevented? What is prognosis like?

A
  • vit E/Se supplementation
  • high-quality forage
  • monitor blood levels regularly

guarded

35
Q

What causes seasonal pasture myopathy? Where is this most commonly seen?

A

seed from Box elder trees contain hypoglycin A, which causes acquired lipid storage myopathy

eastern USA and Europe

36
Q

What are 3 major risk factors to developing seasonal pasture myopathy?

A
  1. season - windy and rainy weather is most common in fall and early spring, making the presence of Box elder tree seeds common on pasture
  2. young horses new to pasture
  3. wooded pasture, >12 hr or wind
37
Q

What are the major signs of seasonal pasture myopathy?

A

sudden onset, rapidly progressive in several horses on pasture:

  • acute muscle weakness, sweating, and fasciculations
  • stiffness, recumbency
  • tachycardia, tachypnea
  • myoglobinuria
  • collapse, death from cardiac/respiratory failure
38
Q

What are 5 things seen on CBC and biochem in patients with seasonal pasture myopathy?

A
  1. increased CK and AST
  2. myoglobinuria
  3. hyperglycemia
  4. lactic acidemia
  5. increased troponin I
39
Q

What are 2 specific signs of seasonal pasture toxicity post-mortem? What is specifically seen in frozen sections?

A
  1. deficiency in multiple acyl CoA dehydrogenase
  2. extensive necrosis and myodegeneration in deep postural, respiratory, and cardiac muscles

marked intracellular lipid accumulation

40
Q

What treatment is recommended for seasonal pasture toxicity? What is prognosis like?

A
  • aggressive fluid therapy
  • DMSO
  • vitamin E and C
  • NSAIDs

< 25% of horses survive

41
Q

What are common causes of traumatic and anesthetic myopathies?

A

TRAUMATIC - fibrotic myopathy

ANESTHETIC - postanesthetic myopathy, malignant hyperthermia

Equine Medicine (33 decks)

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